While hypermethylation is well known for silencing tumor suppressors, it also contributes to genomic instability, fuelling tumorigenesis, inactivating key DNA repair genes, such as hMLH1 and MGMT, GSTP1, and BRCA1, and accelerates mutation accumulation and cancer progression [16]. Interestingly, the methylation status of PTGER1 is not uniform across cancers, highlighting the dynamic ways in which epigenetic landscapes redirect gene expression during disease evolution [17]. Here, BRCA1 is linked to neoplasm.